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Endocrine
For quiz 1 Path 2
| Question | Answer |
|---|---|
| Glands are | Specialized secretory epithelial cells |
| What is the function of glands | synthesis, store and secrete |
| What are the portals of entry | Hematogenous, direct extension, disturbance of growth |
| Endocrine cells act on ______ cells | distant |
| 1 Hypofunction | Not making enough hormone b/c of direct damage |
| 2 Hypofunction | Not making enough hormone b/c of lack of stimulation |
| 1 Hyperfunction | Too much hormone b/c/ of tumor/hyperplasia |
| 2 Hyperfunction | Too much hormone b/c overstimulated from hormone from other organ |
| Examples of 1 Hypofunction | Organ is destroyed, organ not developed, organ is defective |
| Examples of 2 Hypofunction | If pit gland is destroyed/ not developed-> adrenal gland not developed |
| Examples of 1 Hyperfunction | Functional cortical adenoma of adrenal gland, functional thyroid gland adenoma |
| Examples of 2 Hyperfunction | PG- dependent cushings, adrenal gland overstim by tumor in PG |
| Example of hypersecretion of hormone/ hormone like substance by non-endocrine organ | Humoral hypercalcemia of malignancy from PTHrP which is sim to PTH |
| Parts of the Pituitary gland | Adenohypophysis and Neurohypophysis |
| Parts of the Adenohypophysis | Pars Distalis and Pars intermedia |
| Parts of the Neurohypophysis | Pars Nervosa |
| Two cells in Pars Distalis | Acidophils and Basophils |
| Hormones released from Acidophils | Somatotrophs-> Growth hormone (somatotropin) and Lactotrophs (prolactin) |
| Hormones released from Basophils | Corticotroph->ACTH-> cortisol, Thyrotroph->TSH->T3 and T4, Gonadotroph->FSH and LH |
| What type of function is Diabetes Insipidus | Hypofunction |
| What type of function is central Diabetes Insipidus | if tumor, secondary |
| What type of function is nephrogenic Diabetes Insipidus | Primary |
| What type of function is somatotroph adenoma? | Primary hyperfunction |
| What is a clin sign of somatotroph adenoma? | Acromegaly and DM in cats |
| What type of function is corticotroph adenoma at pit gland? | Primary hyperfunction |
| What type of function is corticotroph adenoma at adrenal gland? | Secondary hyperfunction |
| What is a clin sign of corticotroph adenoma? | High blood ACTH w/ bilateral symmetric adrenal gland hyperplasia of ZF and ZR + big pit gland. |
| What type of function is Pit gland carcinoma? Why? | Primary hypofunction, because its non-functional |
| What is a clin sign of Pit gland carcinoma? | Central DI |
| PPID pathogenesis | Compression of hypothalamus from pars intermedia adenoma->dysfunction -> intermittent hyperexia, hirsutism, and polyphagia |
| PPID endocrine pathogenesis | Endocrine active -> increase CLIP, MSH and beta endorphins -> Increase iACTH-> bilateral symmetry of adrenal cortical hyperplasia |
| What type of function is PPID? | Secondary hyperfunction |
| Difference between dog cushings and horse cushings | Dog gets alopecia versus horse does not lose winter coat. |
| What type of function is aplasia and prolonged gestion? | Hypofunction |
| What type of function is a functional adrenal gland tumor? | Primary hyperfunction |
| What type of function is Pit cyst/dwarfism | Primary hypofunction |
| Pit cyst/dwarfism pathogenesis | Fail of pars distalis development -> cyst takes up space-> panhypopituitarism-> hyposomatotropism= no GH |
| Parts of the Adrenal cortex | ZG, ZF, ZR |
| What substances are made from the adrenal cortex | ZG- Mineralcort (Aldosterone) , ZF-Glucocort (Cortisol), ZR- Sex hormones |
| What substances are made from the adrenal medulla | Epi and norepi |
| What type of function is Immune mediated adrenalitis | Primary hypofunction |
| What electrolyte changes do you see in Immune mediated adrenalitis | Decreased NA and increased K |
| What type of function is Pit gland damage | Secondary hypoadrenocrticism |
| What type of function is Pit gland damage | Secondary hypoadrenocrticism |
| What is another name for Immune mediated adrenalitis? | Addisons |
| What electrolyte changes do you see in Iatrogenic or Pit gland damage? | Normal Na or K |
| What zones are under ACTH trophism | ZF and ZR |
| What cortical zones are lost in secondary hypoadrenocorticism? | Both ZF and Zr |
| What cortical zones are lost in Primary hypoadrenocorticism? | All |
| What type of function is Pituitary dependent Cushings? | Secondary hyperadrenocorticism |
| What type of function is Adrenal gland dependent Cushings? | Primary hyperadrenocorticism |
| What clinical signs do you see in Pituitary dependent Cushings? | Bilateral adrenal gland hyperplasia |
| Pituitary dependent Cushings pathogenesis | Functional Pit gland tumor-> Increases ACTH -> increased cortisol raised by ACTH ->excess stim-> ZF and ZR hyperplasia |
| What clinical signs do you see in Adrenal Gland dependent Cushings? | Unilateral cortical atrophy due to tumor on the other adrenal gland. |
| Which cortical zones are lost in Adrenal Gland dependent Cushings? | ZF and ZR on normal adrenal gland |
| Adrenal Gland dependent Cushings pathogenesis | Normal ACTH to start->tumor increases cortisol ->trigggering negative feedback->decreased ACTH |
| Cushings Clinical signs | Polyphagia, distended abdomen, bilateral alopecia, steroid hepatomegaly, cutaneous cutis, immunosupression. |
| Cushings Sequela | Poss UTI |
| What type of function is Conn's syndrome | hyperaldosteronism |
| Conn's syndrome pathogenesis | Uni or bilateral adrenal gland tumor on ZG->increased mineralcort secretions |
| Conn's syndrome electrolytes | Increased Na and decreased K |
| What is the most common medullary tumor? | Pheochromocytoma |
| Normal thyroid gland pathway | Follicular cells stim by TSH-> follicular cells become columnar and releases T3 and T4-> negative feedback back to pit gland |
| C cells | Makes calcitonin when hypercalcemic |
| Which animal gets C-cell tumor | Bulls |
| Three types of hypothyroidism | Thyroid tissue loss, goiter, pit gland pars distalis or hypothalamic lesion |
| Hypothyroid hormones | low T3, T4, Iodine intake, hypercholesteremia, Maybe high TSH |
| Hypothyroid clin signs | Artherosclerosis, weight gain, alopecia, hepatomegaly, hepatic lipidosis, |
| Inherited goiter pathogenesis | Inherited autosomal recessive mutation->abnormal pathway-> decreased production of T3 an T4 w/ increase of TSH-> thyroid cells interact with T3 and T4 but there is no iodothyroine production-> follicular cell hyperplasia |
| Acquired goiter pathogenesis | Hyperplasia due to too much or too little iodine. Also goitergenic substances |
| What animal primarily gets hyperthyroidism | Cats |
| Hyperthyroidism pathogenesis | Functional unilateral or bilateral hyperplasia or adenoma ->increased production of T3 and T4, decreased TSH cause of - feedback |
| Hyperthyroid clinical signs | Weight loss, Triangular shaped face, concentric ventricular hypertrophy, tachycardia |
| If dog has thyroid mass | Prob non-functional carcinoma |
| PTH is released when | hypocalcemic |
| PTH electrolytes normal | Increase Calcium and decrease phosphorus |
| Hypoparathyroidism causes | Diffuse lymphocytic parathyroiditis (Immune), non functional neoplasm, iatrogenic removal, atrophy from sustained hypercalcemia |
| Hypoparathyroidism clin signs | hypocalcemia, hyperphosphatemia -> neuromuscular tetany and excitability and poss seizures |
| If its a primary hyperparathyroidism it will look like? | asymmetrically enlarged glands from tumor |
| If its a Secondary hyperparathyroidism it will look like? | Symmetrically enlarged glands from nutrition or renal |
| What is a nutritional cause of secondary hyperparathyroidism? | Low calcium and high phosphorus |
| What is a renal cause of secondary hyperparathyroidism? | Renal fail -> low D3 and chronic increased phos-> low calcium |
| Causes of pseudohyperparathyroidism? | Carcinoma, lymphoma, anal sac apocrine gland adenocarcinoma, plasma cell myeloma (CLAP) -> secrete PTHrP -> hypercalcemia and normophosphotemia |